Thanks for this, Lookinglass. I will take this with me when we go to see the paed at the end of May. Of course, he will no doubt dismiss it, as he has all of the other studies and info I have shown him, in relation to my daughter's neurological changes when given carbohydrates, which I believe is down to a bacterial overgrowth.

I've not had a chance to fully look at these but there seems to be some work on endro viruses causing auto immune diseases. They seem to relate to myocarditis which I believe is an auto immune heart disease.

They talk of effects on T, B cells as well as activation of cytokines including tumor necrosis factor-a (TNF-a), interleukin (IL)-1, and IL-6. I've seen the levels of some of these discussed in papers on ME although I've no idea how the levels compare.

I think this is on the right track. The word "auto-immune" suggests something of an assumption that the immune system is behaving inappropriately and attacking the body for no reason. This is of course not what the immune system is supposed to do: it is supposed to respond the pathogens. It has long seemed more likely to me that in "auto-immune" diseases the immune system is responding to pathogenic factors that just aren't yet understood. There is clearly collateral damage to parts of the body when this happens, but if the immune system were functioning intelligently, that damage would be preferable to the alternative if the unknown pathogens went unchecked.

It may even be that if the 'auto-immune' response to these unknown pathogens involves genetic factors as well, those genetic factors could actually be strengths rather than weaknesses, as is typically assumed. If the pathogens involved cause serious illnesses - such as cancer - then those without this kind of 'auto-immune' response could be dying from cancers caused by these same pathogens. The activation of tumor necrosis factor seems consistent with this kind of hypothesis. It's just a vague hypothesis, but I suspect the full explanation may be something along these lines. In any case, I think this particular link between 'autoimmune' and bacteria is important and this is a really promising direction for future research.

Mark, your explanation of autoimmune illness is exactly what my doctor said to me recently. He says autoimmunity is very closely associated with chronic infections, and the level of ANA titers varies according to the level of the infection activity.
eg. About ten percent of long term lyme disease patients become auto immune and, of those, the ones who can be cured lose their autoimmunity once the infection is gone.
I am convinced this is what goes on in all the other autoimmune diseases.

1. This is a talk at a conference rather than peer reviewed research
2. The talk provides no meaningful evidence to support its assertions
3. The talk does not relate in any way to CFS/ME
4. The bulk of medical research on both autoimmune disease and autism do not support a contention that they are the result of chronic infection, one word: histocompatibility.

"Our working hypothesis is that immune dysfunction associated with inflammation of the intestinal mucosa leads to the introduction of bacterial components, including neurotoxins, into the bloodstream, creating oxidative stress as well as microvascularities, especially affecting meningeal vessels and finally specific neuronal damage. "

In the case of ME and CFS we have lipopolysaccharides in our blood, but I do not recall seeing this paper published yet (by KDM). There may indeed be a case here, but so far there has been little published. We need these people to publish - one of the issues that is happening I think is that everyone is trying to publish in higher prestige journals, and work their way down till they get accepted. This slows down the research cycle, so its debatable if publishing in high prestige journals is worth it, particularly if they are behind paywalls.High levels of LPS in us should induce toxic shock - but instead we get a different reaction. If that can be confirmed it is certainly very interesting: I wonder if the issue might be different bacterial toxins in different neuroimmune diseases?

Still think bacterial overgrowth is a secondary infection from an enteroviral "hit" in the first place. I cleared the gut with high dose Amoxicillan (for teeth infection) - the virus is a chronic infection.

I find it hard to see how this talk establishes anything relevant to CFS or ME unless you make about twenty assumptions and ignore some pretty rigourous recent research.

Histocompatibility v antigens offer a link between autoimmunity and the target of that autoimmune process.

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You're doing the same thing, Ramakentesh!
You keep throwing out unfounded assertions about the cause of CFS without providing any proof or even a logical hypothesis.
What on earth do you mean by "histocompatibility v antigens"?? That's nonsensical. I've already asked you to explain what you mean, and you haven't.

How am I doing the same thing? Im not really trying to prove anything here.

About 70 years of peer reviewed medical research has established that autoimmune illnesses are associated with certain genetic markers in patients - these genes are usually histocompatibility. HLA-B27 is associated with Ankylosing Spondylitis etc. What seems to occur in these people - and this is based on a myriad of peer-reviewed research is that people seem to acquire autoimmune illnesses that are based on their histocompatibility and perhaps an inability of the innate or b cell immune syste to differentiate between proteins and antigens produced by foreign bodies and infectious bacteria/virus and similar genetic material in the human body.

To explain my points would take me all day in some ways and would require an explanation of current theories on autoimmunity that I cannot really be bothered providing here.

But there are thousands of articles of autoimmunity and molecular mimicry that you could read.

But Im always suprirised -and offer caution - on how people seem to often gravitate to theories that require a set of assumptions to be made to support the contentions (which are usually supporting a pre-conceived idea of what they want to find in terms of etiology). Real science does the opposite.

Doesnt mean that the contentions of the talk are baseless but there are basic tenants of rheumatology that do not support these lines of thought. medical research is nearly always theoretical rather than definitive.

HOWEVER, if you were interested in theories the connection between a bacterial infection of the stomach and the development and potentiation of an inflammatory autoimmune disease in individuals with certain histocompatibility genetic markers you could look at the work of Dr Erbringer on Klebsieba bacteria (the theory being this bacteria releases protein and antigens that mimic the HLA-B27 self antigens and causing the innate immune system to attack these self antigens. Interestingly, despite the resistance against this theory from the wider Rheumatological community, many patients find that low starch diets which by theory would reduce Klebsieba infections remediate symptoms in Chrohns and Ank Spond as examples.

They talk of effects on T, B cells as well as activation of cytokines including tumor necrosis factor-a (TNF-a), interleukin (IL)-1, and IL-6. I've seen the levels of some of these discussed in papers on ME although I've no idea how the levels compare.

Click to expand...

Cytokines are quite different. In some inflammatory diseases there is abherant activation specifically of the innate immune system. It seems interesting that these can be site specific such as in Rheumatoid Arthritis, Ankylosing Spondylitis and inflammatory bowel disease.

Autoimmune hepatitis can be treated with Humira and other TNF alpha blockers, possibly supporting the concept of another site specific innate immune system cytokine elaboration.

Research in this area is focusing on the role of the cytokine mechanisms that suppress TNF alpha activation.

There was even a theory floating around one research body that innate activation suppressed other immune system responsiveness.

How am I doing the same thing? Im not really trying to prove anything here.

About 70 years of peer reviewed medical research has established that autoimmune illnesses are associated with certain genetic markers in patients - these genes are usually histocompatibility. HLA-B27 is associated with Ankylosing Spondylitis etc. What seems to occur in these people - and this is based on a myriad of peer-reviewed research is that people seem to acquire autoimmune illnesses that are based on their histocompatibility and perhaps an inability of the innate or b cell immune syste to differentiate between proteins and antigens produced by foreign bodies and infectious bacteria/virus and similar genetic material in the human body.

To explain my points would take me all day in some ways and would require an explanation of current theories on autoimmunity that I cannot really be bothered providing here.

But there are thousands of articles of autoimmunity and molecular mimicry that you could read.

But Im always suprirised -and offer caution - on how people seem to often gravitate to theories that require a set of assumptions to be made to support the contentions (which are usually supporting a pre-conceived idea of what they want to find in terms of etiology). Real science does the opposite.

Doesnt mean that the contentions of the talk are baseless but there are basic tenants of rheumatology that do not support these lines of thought. medical research is nearly always theoretical rather than definitive.

HOWEVER, if you were interested in theories the connection between a bacterial infection of the stomach and the development and potentiation of an inflammatory autoimmune disease in individuals with certain histocompatibility genetic markers you could look at the work of Dr Erbringer on Klebsieba bacteria (the theory being this bacteria releases protein and antigens that mimic the HLA-B27 self antigens and causing the innate immune system to attack these self antigens. Interestingly, despite the resistance against this theory from the wider Rheumatological community, many patients find that low starch diets which by theory would reduce Klebsieba infections remediate symptoms in Chrohns and Ank Spond as examples.

As always, Google is a wonderful resource.

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Thanks you for your explanation, Ramakentesh.
The only reason I was getting irritated was because you didn't explain before, I certainly would not be irritated by hearing your ideas explained.
How would your ideas fot with the pattern of autoimmunity in Lyme disease? It often triggers elevated levels of ANA titers which at first cannot be linked to any specific organ. Over time, as it worsens I suppose, immune activity can be identified as celiac disease in some, Hashimoto's thyroiditis and others, and various other autoimmune diseases. It seems to be random about which organ it targets in which patient.

Perhaps in Lyme the pathogens are able to trick the immune system into attack self antigens over pathogenic antigens. This does occur with some stomach worms who are able to excude proteins that suppress proinflammatory cytokines. Lyme is pretty confusing and it apparently has specific types of neuropathic damage traits that some can detect.
There may even be an epigenetic mechanism in some or just a propensity to suffer autoimmunity and then the type or target is perhaps dictated by histocompatibility genes (or so they think).